In addition, several studies have shown that high levels of SUA can activate oxidative stress and inflammatory stress, such as activation and enhancement of interleukin-1 β, cyclooxygenase-2, reactive oxygen species and renin-angiotensin system, thus promoting endothelial dysfunction, which may eventually lead to an increase in the risk of death (22, 23). Here, PTGS2 is linked to endothelial dysfunction.